World Journal Of Biological Chemistry[JOURNAL]
Sun
200 papers
Single-cell deoxyribonucleic acid typing for forensic mixtures and trace evidence: Opportunities, validation requirements, and reporting limits.
Evangelou K, Angeli P, Polydorou A … +1 more , Petropoulou T
World J Biol Chem · 2026 Jun · PMID 42273528 · Full text
Forensic deoxyribonucleic acid (DNA) interpretation is limited less by genotyping technology than by the biochemical and inferential effects of mixed, low-template, and environmentally complex traces. Single-cell and sin...
Forensic deoxyribonucleic acid (DNA) interpretation is limited less by genotyping technology than by the biochemical and inferential effects of mixed, low-template, and environmentally complex traces. Single-cell and single-molecule strategies, including the United Kingdom Research and Innovation-funded single-cell and single-molecule analysis for DNA identification (SCAnDi) program, aim to preserve cellular resolution. They allow investigators to isolate and type individual cells or defined small-cell pools before heterogeneous evidence is converted into a bulk lysate. In selected validation settings, this approach has yielded near-complete diploid short tandem repeat (STR) profiles from small pools, credible genotype sets tightly concentrated on the true genotype across high-order mixtures, and improved access to donor-specific profiles from sexual assault and other complex samples. However, these studies also show important limits. Many operationally successful "single-cell" workflows are, in practice, single-cell-plus-consensus or few-cell workflows. Stochastic effects remain intrinsic, and cell capture itself becomes a probabilistic sampling step. This opinion review explicitly adopts an evaluative stance: It synthesizes recent validation studies and guidance documents to identify the performance thresholds and reporting boundaries that should be met before targeted forensic deployment of SCAnDi-like workflows. We argue that casework entry should require measured cell-recovery probabilities, phenotype-misclassification rates, locus- and cell-type-specific dropout and stutter models, quantified contamination and drop-in rates, validated minimum cell counts for consensus generation, and explicit database-upload criteria. It should also require strict separation between sub-source reporting and activity-level propositions. If those conditions are met, single-cell typing can complement, rather than replace, bulk STR analysis and probabilistic genotyping in a narrow but important set of high-value forensic scenarios.
Glycemic status, antioxidant enzyme and lipid peroxidation among patients with diabetes mellitus in Buea Regional Hospital in Cameroon.
Ojong EW, Nyake Mbu Akime LB, Tambe AB … +4 more , Seukep AJ, Ofon EA, Akwa TC, Sawah CN
World J Biol Chem · 2026 Jun · PMID 42273527 · Full text
BACKGROUND: Oxidative stress has been suggested to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM) and development of complications by altering antioxidant levels and inducing lipid peroxidation. Altho...
BACKGROUND: Oxidative stress has been suggested to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM) and development of complications by altering antioxidant levels and inducing lipid peroxidation. Although patients with T2DM are reported to be under oxidative stress because of prolonged exposure to hyperglycemia, the influence of glycemic control in diabetes on enhanced free-radical activity is poorly understood. AIM: To evaluate the levels of malondialdehyde (MDA) - a marker of lipid peroxidation and catalase (CAT) - an antioxidant enzyme in patients with T2DM categorized by glycemic control, and to compare these levels with those of apparently healthy individuals in Buea, Cameroon. METHODS: A hospital-based case-control study was conducted at Buea Regional Hospital from January 2024 to June 2024 involving patients with T2DM and age-matched healthy controls. Socio-demographic, clinical and anthropometric data were collected using a structured questionnaire. Levels of glucose, lipid profile, CAT and MDA were determined by spectrophotometry. Glycated hemoglobin was measured using ion exchange high performance liquid chromatography method. Data analyses were done using IBM SPSS version 26.0 for Windows. A ≤ 0.05 was considered statistically significant. RESULTS: A total of 192 participants (96 patients with T2DM and 96 healthy controls) were recruited in this study. The mean age of the participants was were 47.97 ± 10.3 years with most being males (62.5%). CAT activity and high-density lipoprotein cholesterol levels were higher in control subjects ( < 0.05). The majority of patients with T2DM (80.2%) had a poor glycemic control. CAT activity was lower and MDA was significantly higher in patients with T2DM with poor glycemic control ( < 0.001). Glycated hemoglobin showed a significantly strong positive correlation with MDA levels ( = 0.846, < 0.001) and a significantly strong negative correlation with CAT activity ( = -0.567, < 0.001). Additionally, there was a significant negative correlation between CAT activity and MDA ( = -0.568, < 0.001). CONCLUSION: The results of this study indicated a significantly higher level of MDA and lower CAT activity in patients with T2DM compared to apparently healthy age-matched and sex-matched controls. Increased lipid peroxidation and decrease antioxidant enzyme activity were associated with poor glycemic control. The correlation between lipid peroxidation, antioxidant activity, and glycemic control highlights the role of oxidative stress in the pathophysiology of T2DM.
Study of stem and leaf and pods: An therapeutic approach for leukemia.
Boro A, Jothi Dheivasikamani A, Prabhu Jeyabal Philomenathan A … +4 more , Manivannan J, Krishnaswamy S, Palanisamy S, Arumugam VA
World J Biol Chem · 2026 Jun · PMID 42273526 · Full text
BACKGROUND: () Miers is an evergreen and dioecious herb of the Menispermaceae family. () Lam. is a medium-sized tree of the Fabaceae family, and it is known for its nutritional, economic, and medicinal importance. AIM:...
BACKGROUND: () Miers is an evergreen and dioecious herb of the Menispermaceae family. () Lam. is a medium-sized tree of the Fabaceae family, and it is known for its nutritional, economic, and medicinal importance. AIM: To analyze the phytochemicals and enzymes in and and perform an therapeutic assay. METHODS: The phytochemical compounds in stem aqueous extract (TCAE), leaf aqueous extract (SLAE), and pod aqueous extract (SPAE) were estimated. Activity of catalase, superoxide dismutase, peroxidase, polyphenol oxidase, and ascorbate oxidase was quantified in protein extracts from stem, leaf, and pods, and an therapeutic assay was performed in THP-1 cells. RESULTS: Quantitative analysis revealed that the total flavonoid content was high in SLAE. The total phenolic compound content was high in SLAE. The total tannin content was high in SPAE. The enzymatic activity of catalase, peroxidase, and ascorbate oxidase was high in stem, and the enzymatic activity of superoxide dismutase and polyphenol oxidase was high in pods. TCAE, SLAE, and SPAE induced THP-1 cell apoptosis due to an increase in reactive oxygen species and a decrease in mitochondrial membrane potential activity. CONCLUSION: and may have therapeutic potential in leukemia, but further clinical studies are needed.
Triggering receptor expressed on myeloid cells 2-driven pancreatic macrophage crosstalk: Key regulator of obesity pathophysiology and metabolic dysregulation.
Zhang AY, Xie CY, Song X … +6 more , Guo ZH, Shi YR, Wang SY, Yang GH, Liu Y, Xu TC
World J Biol Chem · 2026 Jun · PMID 42273525 · Full text
Obesity, a global epidemic, is closely linked to metabolic complications like insulin resistance and type 2 diabetes. Pancreatic dysfunction (impaired islet secretion and local inflammation) is central to this deteriorat...
Obesity, a global epidemic, is closely linked to metabolic complications like insulin resistance and type 2 diabetes. Pancreatic dysfunction (impaired islet secretion and local inflammation) is central to this deterioration, yet the underlying mechanisms remain unclear. Pancreatic macrophages regulate tissue inflammation and metabolic homeostasis, but their context-specific polarization in obesity is undefined. This review discusses the role of triggering receptor expressed on myeloid cells 2 (TREM2) in modulating pancreatic macrophage behavior in the context of obesity, based on findings from diet-induced obese mouse models and pancreatic analyses. Emerging evidence indicates that TREM2 expression is markedly upregulated in pancreatic macrophages of obese subjects, where TREM2-driven macrophage activation promotes pro-inflammatory cytokine release and disrupts macrophage-islet β-cell crosstalk. Transcriptomic profiling reveals that TREM2 signaling reshapes macrophage transcriptional landscapes, enhancing pro-inflammatory phenotypes while impairing islet-supporting capacity. Notably, macrophage-specific TREM2 ablation has been shown to ameliorate pancreatic inflammation, restore islet insulin secretion, and alleviate systemic metabolic disorders in obese mice. Collectively, these findings identify TREM2 as a pivotal molecular switch governing pancreatic macrophage-mediated metabolic dysfunction in obesity, highlighting TREM2 pancreatic macrophages as a potential therapeutic target. These findings advance the understanding of immune-metabolic crosstalk in the pancreas, laying a foundation for developing novel immunometabolic interventions.
Precore/core mutation relatedness to viral reactivation in patients undergoing targeted therapy for hepatitis B virus-related hepatocellular carcinoma.
Abdulrahman MS, Aboelmagd O, Zhang Y … +2 more , Zaky S, Johar D
World J Biol Chem · 2026 Jun · PMID 42273524 · Full text
Hepatitis B virus (HBV) reactivation after targeted therapy or immunomodulating therapy leads to active or fulminant hepatitis, low response to prophylactic vaccination, premature discharge from therapy and death. The hy...
Hepatitis B virus (HBV) reactivation after targeted therapy or immunomodulating therapy leads to active or fulminant hepatitis, low response to prophylactic vaccination, premature discharge from therapy and death. The hypothesis that seroreactive viral infection is caused by mutation/s in the precore/core is invaluable to elucidating the mechanisms of HBV reactivation. Precore/core mutations may correlate with, or predict susceptibility to seroreactivation in HBV-related hepatocellular carcinoma (HCC) patients receiving targeted therapy. This review's objective is to re-analyze the relationship between the precore/core mutations of HBV-DNA and HBV reactivation in HCC patients receiving targeted therapy. Further, to re-analyze clinically significant precore/core mutations affecting pregenomic RNA initiation and synthesis, and their regulation of viral and cellular gene expressions. This review shed light on the mechanism of HBV reactivation. We analyze the effects of antivirals lamivudine, entecavir, tenofovir alafenamide, tenofovir disoproxil fumarate and immune-based strategies on reactivation after treatment for HBV-related HCC. We proposed future directions for studying mutations in the precore/core region that are likely to cause relapse. This review recommends comparing the genome/proteome of blood from overt and relapsed HCC-related chronic HBV patients. This helps identifying persistent genetic/epigenetic profiles of HBV resistant variants, thus accurately selecting the appropriate antiviral therapy and eliminating the risk of viral reactivation.
Phytosterols in human health: Biochemical mechanisms of action and disease-modulating effects.
Mohamed D, Ramadan AA, Mabrok HB … +1 more , Hamed I
World J Biol Chem · 2026 Jun · PMID 42273523 · Full text
Phytosterols are plant-derived sterols structurally similar to cholesterol and present in vegetable oils, seeds, legumes, and whole grains. Their best-established health effect is lowering circulating low-density lipopro...
Phytosterols are plant-derived sterols structurally similar to cholesterol and present in vegetable oils, seeds, legumes, and whole grains. Their best-established health effect is lowering circulating low-density lipoprotein cholesterol, mainly through inhibition of intestinal cholesterol absorption. Beyond this classical role, recent studies suggest that phytosterols may influence biological processes relevant to human health. Proposed mechanisms include changes in membrane lipid organization, modulation of nuclear receptors such as liver X receptors and peroxisome proliferator-activated receptors, activation of AMP-activated protein kinase, and regulation of metabolic and inflammatory signaling pathways. Experimental and human evidence indicates possible effects on adipose tissue function, hepatic lipid accumulation, insulin sensitivity, inflammation, oxidative stress, and immune responses. These findings have increased interest in the relevance of phytosterols to obesity, metabolic dysfunction-associated steatotic liver disease, type 2 diabetes, and immune-mediated disorders such as rheumatoid arthritis. Interactions with the gut microbiota and bile acid metabolism may provide additional pathways linking phytosterol intake with systemic effects, although human evidence remains limited. Antioxidant and anti-inflammatory actions have also been linked to neuroprotective and anticancer effects, but current support is mainly from preclinical studies. This review critically summarizes mechanistic and translational evidence, with emphasis on bioavailability, interindividual variability, safety, and remaining research gaps.
Clinical utility of human leukocyte antigen genotyping and immunoglobulin G4 autoantibody testing in autoimmune neurological diseases: A focused minireview.
Bouayad A
World J Biol Chem · 2026 Mar · PMID 41884075 · Full text
The diagnosis of immunoglobulin G4 (IgG4)-related autoimmune neuropathies relies on a combination of clinical evaluation, imaging, and biological analyses, including serum and cerebrospinal fluid assessments. Several IgG...
The diagnosis of immunoglobulin G4 (IgG4)-related autoimmune neuropathies relies on a combination of clinical evaluation, imaging, and biological analyses, including serum and cerebrospinal fluid assessments. Several IgG4 autoantibodies have been described in these disorders, including muscle-specific kinase IgG4, leucine-rich glioma-inactivated 1 IgG4, nodo-paranodal IgG4, Ig-like domain-containing protein 5, anti-dipeptidyl-peptidase-like protein-6 antibodies, and contactin-associated protein-like 2 IgG4. Accurate identification of these autoantibodies using appropriate techniques is essential for optimizing diagnosis and guiding treatment selection. In addition, specific human leukocyte antigen (HLA) alleles and haplotypes are associated with the induction of these autoantibodies. This review summarizes current knowledge on the role of HLA alleles in regulating IgG4 autoantibody production and examines methods for detecting these autoantibodies, as well as their diagnostic and prognostic significance in IgG4-mediated neurological disorders.
Dithiothreitol induced endoplasmic reticulum stress and its role in neurodegeneration in .
Raj G, Kumar M, Shreya S … +4 more , Bhardwaj S, Priya R, Mangalhara KC, Jain BP
World J Biol Chem · 2025 Dec · PMID 41378254 · Full text
BACKGROUND: Neurodegeneration refers to the progressive loss of neurons, affecting both their structure and function. It is driven by synaptic dysfunction, disruptions in neural networks, and the accumulation of abnormal...
BACKGROUND: Neurodegeneration refers to the progressive loss of neurons, affecting both their structure and function. It is driven by synaptic dysfunction, disruptions in neural networks, and the accumulation of abnormal protein variants. Endoplasmic reticulum (ER) stress, caused by the accumulation of misfolded or unfolded protein, is a major contributor to neurodegeneration. Dithiothreitol (DTT) is a widely used redox reagent that disrupts the oxidative protein folding environment, inducing ER stress and leading to the imbalance in protein homeostasis can activate stress response pathway, potentially contributing to neurodegenerative processes. () is a widely used model organism for studying neurodegeneration due to its well-mapped nervous system, approximately one-third of neuron cells in their body, complete genome sequenced, and conserved stress response pathway. AIM: To study the neurodegeneration in caused by DTT-induced ER stress, assessed by behavioral, molecular, and lifespan changes. METHODS: were cultured on nematode growth medium plates with OP50, and ER stress was induced using DTT. Effects were assessed behavioral assays such as locomotion, chemotaxis, lifespan assay, and molecular studies. RESULTS: DTT exposure led to a significant decline in locomotion and chemotaxis response, indicating neurotoxicity. A reduction in lifespan was observed, suggesting an overall impact on health. Molecular analysis confirmed ER stress activation. DTT-induced ER stress negatively affects , leading to behavioral impairments and molecular alterations associated with neurodegeneration. CONCLUSION: These findings establish as a potential model for studying ER stress-mediated neurotoxicity and its implications in neurodegenerative diseases.
Interferon-gamma signaling pathway: Modulation of key genes in the progression of glioblastoma.
Oropeza-Martínez E, Palacios Serrato EG, Zamora-Salas SX … +4 more , Lira-Rodríguez NA, López-Mignon SH, Martinez-Benitez MB, Tecalco-Cruz AC
World J Biol Chem · 2025 Dec · PMID 41378253 · Full text
The canonical signaling of interferon gamma (IFN-γ) through the Janus kinase 1 and 2-signal transducer and activator of transcription 1 (STAT1) axis leads to the expression of several interferon-stimulated genes (ISGs),...
The canonical signaling of interferon gamma (IFN-γ) through the Janus kinase 1 and 2-signal transducer and activator of transcription 1 (STAT1) axis leads to the expression of several interferon-stimulated genes (ISGs), which have diverse effects depending on the cellular context. In glioblastoma, a highly aggressive primary brain tumor in adults, elements of IFN-γ canonical signaling are deregulated, resulting in the overexpression of STAT1-target ISGs associated with tumor progression. This mini-review highlights key ISGs, including , interferon regulatory factor 1, programmed death-ligand 1, indoleamine 2,3-dioxygenase 1, and interferon-stimulated gene 15, involved in the pathology of glioblastoma. These genes may serve as valuable biomarkers and have therapeutic potential for targeting IFN-γ signaling in this malignancy.
Fatty liver reexamined choline and mitochondrial toxin amelioration.
Mercola J
World J Biol Chem · 2025 Dec · PMID 41378252 · Full text
Choline supports phospholipid synthesis, membrane integrity, neurotransmission, verylowdensity lipoprotein export, and one-carbon/epigenetic pathways, yet most United States adults fall short of adequate intake. Fatty li...
Choline supports phospholipid synthesis, membrane integrity, neurotransmission, verylowdensity lipoprotein export, and one-carbon/epigenetic pathways, yet most United States adults fall short of adequate intake. Fatty liver is now viewed as a mitochondrial-centric metabolic-inflammatory disorder; ethanol and excess linoleic acid (LA) can magnify bioenergetic stress when choline is insufficient to sustain phosphatidylcholine/phosphatidylethanolamine. This narrative review examines whether optimized choline delivery, alongside reduced exposure to mitochondrial toxicants, offers a rational therapeutic approach. Low choline intake associates with higher liver fat and aminotransferases. In rodents, choline deficiency combined with ethanol or LA lowers mitochondrial membrane potential, limits β-oxidation, and promotes steatosis and inflammation. Advanced formulations-especially citicoline-demonstrate favorable absorption and tissue choline delivery and may lessen trimethylamine-N-oxide formation versus free choline salts. Early, small human studies suggest that choline repletion, together with curtailed ethanol or dietary LA, can reduce intrahepatic triglyceride content and improve insulin sensitivity, though large randomized trials are lacking. Framing fatty liver as nutrition-modifiable mitochondrial toxicosis highlights correctable choline insufficiency when the liver is burdened by ethanol or excess LA. A dual strategy-using higher-bioavailability, gutmicrobial trimethylamineNoxide-sparing choline forms and mitigating mitochondrial toxicants-targets core bioenergetic defects, may reverse early steatosis, and warrants testing in adequately powered clinical trials.
Molecular and cellular mechanisms of pentadecanoic acid.
Mercola J
World J Biol Chem · 2025 Dec · PMID 41378251 · Full text
Pentadecanoic acid (C15:0) is an odd-chain fatty acid, the β-oxidation of which yields propionyl-CoA that replenishes succinyl-CoA and tricarboxylic acid cycle flux; higher circulating levels are associated with reduced...
Pentadecanoic acid (C15:0) is an odd-chain fatty acid, the β-oxidation of which yields propionyl-CoA that replenishes succinyl-CoA and tricarboxylic acid cycle flux; higher circulating levels are associated with reduced type 2 diabetes, cardiovascular disease, metabolic dysfunction-associated steatotic liver disease, and mortality. Summarize the cellular and molecular mechanisms underlying these associations. A comprehensive literature search (2000-2025) identified studies of C15:0's mechanistic actions and , and multi-omics studies focused on receptor binding, signaling cascades, gene expression, and comparative pharmacology. C15:0 is a dual partial peroxisome proliferator-activated receptor α/δ agonist. It activates AMP-activated protein kinase, suppresses mechanistic target of rapamycin, and selectively inhibits histone deacetylase 6. It augments succinate-driven complex II respiration, preserves mitochondrial membrane potential, limits reactive oxygen species, and attenuates interleukin-6 (IL-6) - triggered Janus kinase 2/signal transducer and activator of transcription 3 and nuclear factor kappa B p65 signaling, lowering monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and IL-6. Across the BioMAP human-primarycell platform - which tests 12 distinct primary human cell systems such as endothelial cells, fibroblasts, macrophages, and T-cells - C15:0 (17 µM) produced statistically significant changes in 36 mechanistically diverse biomarkers. This broad, multi-pathway modulation mirrors the phenotype produced by metformin and rapamycin, yet occurred with no detectable cytotoxicity, paralleling metformin and rapamycin with negligible cytotoxicity. C15:0 engages receptor targets that converge on enhanced lipid oxidation, cellular energetics, and inflammation resolution. Although prospective clinical outcomes are still lacking, the pleiotropic mechanism profile positions C15:0 as a potentially unique nutraceutical or adjunct therapeutic candidate. Further research is warranted to confirm its clinical impacts, optimize dosing, and clarify long-term safety as an essential fatty acid supporting metabolic and immune homeostasis.
Association between Alzheimer's disease and products in murine models: A systematic review.
Ochoa KL, Heredia AG, Piedra CC … +3 more , Arias RJ, Ortiz BJ, Dominguez-Gortaire JA
World J Biol Chem · 2025 Dec · PMID 41378250 · Full text
BACKGROUND: Alzheimer's disease is a neurodegenerative dementia characterized by accumulation of β-amyloid plaques, tau hyperphosphorylation, and neuroinflammation. Recent research has highlighted a potential relationshi...
BACKGROUND: Alzheimer's disease is a neurodegenerative dementia characterized by accumulation of β-amyloid plaques, tau hyperphosphorylation, and neuroinflammation. Recent research has highlighted a potential relationship between chronic oral infections and neurodegeneration, particularly the involvement of (), a key pathogen in periodontitis. Experimental mouse models have been used to explore how products contribute to neuroinflammatory and degenerative processes. However, a comprehensive synthesis of these findings is lacking. This systematic review evaluates the role of -derived factors in triggering Alzheimer's-like pathology, with an emphasis on bacterial products and host immune responses. We hypothesize that products exacerbate neuroinflammation and pathology in mouse models of Alzheimer's disease. AIM: To link gingival bacteria-associated products with the onset and progression of Alzheimer's disease-like pathology in mouse models. METHODS: This systematic review followed the 2020 PRISMA guidelines. A comprehensive search was conducted in five databases (PubMed, Scopus, ScienceDirect, Sage, SpringerLink) for original studies between 2014 and 2024. Studies included mouse models to evaluate the effect of or its products on Alzheimer's-like pathologies. Exclusion criteria were , human, or review studies. Twenty-three studies met the inclusion criteria. Bacterial components and activated host factors were extracted, categorized, and analyzed using narrative synthesis and descriptive statistics. RESULTS: In 24 studies, lipopolysaccharides (54.84%) and gingipains (25.81%) were the most frequently reported P. gingivalis products. These factors activated toll-like receptors (TLR2/TLR4), microglia, and astrocytes, increasing levels of interleukin 1 beta, tumor necrosis factor-alpha, and other proinflammatory cytokines. The host response included β-amyloid accumulation, Tau hyperphosphorylation, and changes in blood-brain barrier permeability. Glial cells were the most frequently mentioned host factors ( = 15), followed by proteins ( = 13) and cytokines ( = 11). These interactions promoted cognitive impairment, synaptic dysfunction, and neurodegeneration in mouse models, supporting a role for in Alzheimer's-like pathology. CONCLUSION: products induce neuroinflammatory responses and Alzheimer's-like pathology in mouse models, supporting their role as contributors to neurodegeneration and potential targets for preventive strategies.
Macrophage-mediated metabolic dysregulation in the pancreas: Insights from obesity.
Chen KR, Chen ZY, Liu FY … +5 more , Xie CY, Hu J, Wang SY, Xu B, Xu TC
World J Biol Chem · 2025 Dec · PMID 41378249 · Full text
Obesity is a major contributor to metabolic dysfunction, and its impact on pancreatic health has garnered increasing attention. Macrophages, as key regulators of inflammation and metabolism, play a central role in mediat...
Obesity is a major contributor to metabolic dysfunction, and its impact on pancreatic health has garnered increasing attention. Macrophages, as key regulators of inflammation and metabolism, play a central role in mediating obesity-induced pancreatic damage. In obese individuals, excessive lipid accumulation and chronic low-grade inflammation drive the infiltration and polarization of macrophages within the pancreas. These macrophages, particularly the pro-inflammatory Macrophage, pro-inflammatory phenotype (M1) phenotype, secrete cytokines such as C-C motif ligand 2 (CCL2) and transforming growth factor beta (TGF-β), which disrupt pancreatic β-cell function and impair insulin secretion. Conversely, anti-inflammatory Macrophage, anti-inflammatory phenotype (M2) macrophages contribute to tissue repair but may also promote fibrotic changes under prolonged metabolic stress. Pancreatic macrophages are activated under high-fat diet conditions, promoting inflammation and impairing β-cell function through the SUCLA2-HIF-1α axis and mechanistic Target of Rapamycin Complex 1 (mTORC1)/PD-1 pathway, thereby establishing a self-perpetuating "metabolic-immunosuppressive" vicious cycle. Targeted intervention strategies against macrophages-such as SUCLA2 inhibitors can ameliorate metabolic dysregulation. Meanwhile, exosome-mediated interorgan communication [, microRNA-155 (miR-155) and miR-30a] offers novel insights for multi-system synergistic therapies. Understanding the mechanisms by which macrophages mediate metabolic dysregulation in the pancreas under obese conditions provides critical insights into the pathogenesis of obesity-related pancreatic disorders.
Gut microbiome and chemotherapy-induced cardiotoxicity: A systematic review of evidence and emerging therapies.
Abdulaal R, Afara I, Harajli A … +8 more , Al Mashtoub E, Tarchichi A, Hassan K, Afara A, Abou Fakher J, Salhab S, Fassih I, Tlais M
World J Biol Chem · 2025 Dec · PMID 41378248 · Full text
BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key m...
BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), in mediating inflammation, oxidative stress, and cardiac damage. The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction. AIM: To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients. METHODS: A systematic literature search was conducted in PubMed, Scopus, and Web of Science for studies published between January 2013 and December 2024. Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition, microbial metabolites (, SCFAs, TMAO), or microbiome-targeted interventions. Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Data extraction focused on microbiota alterations, mechanistic pathways, cardiac outcomes, and quality assessments using standardized risk-of-bias tools. RESULTS: Eighteen studies met the inclusion criteria. Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains. This imbalance contributed to gut barrier disruption, systemic inflammation, and oxidative stress, all of which promote myocardial damage. SCFA depletion weakened anti-inflammatory responses, while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction. Preclinical studies showed promising cardioprotective effects from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, though human data remain limited. CONCLUSION: Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity. Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury. Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology, warranting further clinical validation through well-designed trials.
fatty-acid-transporter gene variants- G/A (rs1761667) and C/T (rs75326924) as biomarkers for risk-prediction in gestational diabetes mellitus.
Shamsad A, Gautam T, Singh R … +1 more , Banerjee M
World J Biol Chem · 2025 Dec · PMID 41378247 · Full text
BACKGROUND: Gestational diabetes mellitus (GDM) is a metabolic disorder causing hyperglycemia during pregnancy. Insulin resistance and decreased insulin secretion are linked to altered lipid metabolism that leads to prog...
BACKGROUND: Gestational diabetes mellitus (GDM) is a metabolic disorder causing hyperglycemia during pregnancy. Insulin resistance and decreased insulin secretion are linked to altered lipid metabolism that leads to progression of GDM. CD36 is a membrane glycoprotein involved in lipid metabolism and insulin sensitivity. Studies indicate that the gene is substantially linked to type 2 diabetes mellitus (T2DM) and could also influence GDM susceptibility. Insulin resistance and decreased insulin secretion are the hallmarks of T2DM, which is thought to have a similar genetic pathophysiology in GDM. AIM: To investigate the impact of gene polymorphisms [rs1761667 (G/A) and rs75326924 (C/T)] and mRNA expression in GDM women. METHODS: The case-control study involved a total of 400 pregnant women, (200 healthy controls and 200 GDM cases). The study of gene polymorphisms G/A (rs1761667) and C/T (rs75326924)) were determined by polymerase chain reaction-restriction fragment length polymorphism. The mRNA expression study of gene was analyzed by quantitative polymerase chain reaction/quantitative real-time polymerase chain reaction followed by statistical analysis done using GraphPad Prism8 software (ver. 8.0). RESULTS: The study revealed statistically significant association ( < 0.05) in anthropometric/biochemical parameters (age, gestational age, body mass index, fasting prandial glucose, post-prandial glucose, triglyceride, low-density lipoprotein) between GDM cases and healthy controls. G/A(rs1761667) and C/T (rs75326924) polymorphisms were significantly associated with GDM cases. The heterozygous genotypes (GA and CT) of both variants showed significant association ( = 0.0001 and = 0.0025, odds ratio = 2.683 and 2.022 respectively). Allele frequency of 'T' allele in C/T (rs75326924) polymorphism was also found to be significant ( = 0.0046). gene was upregulated in individuals with GDM as compared to healthy controls ( = 0.0001). However, the upregulation of gene expression was not significantly associated with the genotypes of G/A (rs1761667) and C/T (rs75326924) polymorphisms. CONCLUSION: Heterozygous genotypes GA and CT of gene variants and expression are linked to GDM, potentially serving as predictive biomarkers for GDM susceptibility; further exploration needed in diverse ethnic communities.
Intramuscular injection of therapeutic botulinum toxin facilitates blood coagulation in experimental aging mice.
Ravichandran S, Joseph JHM, Sellathamby S … +1 more , Kandasamy M
World J Biol Chem · 2025 Dec · PMID 41378246 · Full text
BACKGROUND: Botulinum toxin (BoNT) is a bacterial poison that acts by blocking the release of acetylcholine-containing vesicles at the neuromuscular junction. Notably, a mild amount of BoNT is known to exert therapeutic...
BACKGROUND: Botulinum toxin (BoNT) is a bacterial poison that acts by blocking the release of acetylcholine-containing vesicles at the neuromuscular junction. Notably, a mild amount of BoNT is known to exert therapeutic benefits against various diseases, including migraine, movement disorders, anxiety and neurocognitive deficits. BoNT treatment appears to increase platelet count in circulation. Therefore, BoNT treatment may be associated with the regulation of blood coagulation upon haemorrhagic events. However, the effects of BoNT on the degree of bleeding and clotting events have not yet been determined. AIM: To investigate the effect of BoNT on the bleeding parameters and blood coagulation events in experimental mice. METHODS: A group of 7-8-month-old mice was intramuscularly injected with a mild single dose of BoNT. After a month of BoNT injection, animals were subjected to tail bleeding assay, assessment of clotting time, and degree of platelet aggregation in comparison with the control group. RESULTS: Results revealed that BoNT injection significantly reduced blood loss and bleeding time in experimental aging mice upon tail tip transection. Moreover, the blood samples collected from the BoNT-treated mice showed enhanced platelet aggregation and intense formation of the fibrin clot compared to the control. This study indicates a putative therapeutic value of BoNT in mitigating bleeding episodes, possibly through its platelet-enhancing property. CONCLUSION: BoNT treatment effectively facilitates blood coagulation. Upon further validation, this approach can be translated to treat traumatic blood vessel injuries, haemorrhagic diseases, and bleeding complications associated with surgical procedures.
Chemical composition differences in wild fruits across provenances using metabolomics.
Bi WY, He WL, Wang W … +3 more , Wang XR, Zhou ZJ, Zeng YL
World J Biol Chem · 2025 Sep · PMID 40933290 · Full text
BACKGROUND: Fruits of () have extremely high medicinal value. However, the quality and traits of the plants vary significantly based on their provenances. In addition, the behaviour of the known bioactive components, su...
BACKGROUND: Fruits of () have extremely high medicinal value. However, the quality and traits of the plants vary significantly based on their provenances. In addition, the behaviour of the known bioactive components, such as geniposide and crocin, has been the primary focus of the research on . However, the identification of unknown bioactive components and their metabolomics remains underexplored. Therefore, analysing the metabolic differences between gardenias from different sources is essential to provide a comprehensive theoretical basis for the evaluation of and germplasm resource identification. AIM: To systematically evaluate the morphology, secondary metabolites, typical active ingredients, and antioxidant activity of wild fruits. METHODS: Gardenia fruits were collected from different provenances. Metabolites were identified ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The metabolic differences were compared using hierarchical cluster analysis (HCA). The antioxidant capacity was evaluated using 2,2-diphenyl-1-picrylhydrazyl radical scavenging assays and ferric reducing antioxidant power assays, and its correlation with typical active ingredients was analysed. RESULTS: A total of 444 and 240 metabolites were identified using UPLC-MS/MS in positive and negative ion modes, respectively. The HCA results of the flavonoids indicated that the higher content of flavonoids was in the fruits from Lukou. The differential analysis of metabolites in fruits from Shaoyang, Miluo and Lukou showed that the fruit from Miluo had the highest upregulated differential metabolites. CONCLUSION: The metabolic characteristics of the Ningxiang and Xiangxi extracts were similar, while those of Lukou, Miluo and Shaoyang extracts differed significantly.
CD47/SIRPα pathways: Functional diversity and molecular mechanisms.
Bhardwaj N, Chandra H, Singh A … +1 more , Babu R
World J Biol Chem · 2025 Sep · PMID 40933289 · Full text
Cellular communication is required for the normal function and maintenance of homeostasis. The extracellular communications are mediated by cell surface receptors, which transmit signals for various cell functions. Cell...
Cellular communication is required for the normal function and maintenance of homeostasis. The extracellular communications are mediated by cell surface receptors, which transmit signals for various cell functions. Cell defense also relies on distinguishing between self and non-self. The integrins belong to the transmembrane receptors family and serve a crucial function in cell-extracellular adhesion and cell-cell signaling. The cell surface integrin-associated protein, or CD47, is an important integrin regulator and performs an array of functions. The CD47 interacts with the signal regulatory protein α (SIRPα) and regulates adhesion, apoptosis, phagocytosis, proliferation, metabolism, activation, hematopoietic stem cell migration, and malignancies. The CD47 expression is increased in tumor cells to escape immune response. The anti-CD47 antibodies have shown promising therapeutic strategies in various clinical trials in the treatment of hematologic and solid tumors. In the current review, we discussed multifunctional roles, molecular mechanisms, and therapeutic strategies of tumors by utilizing CD47/SIRPα interactions.
Innate immunity and wound repair: The platelet-rich fibrin advantage.
Mohammadi S
World J Biol Chem · 2025 Jun · PMID 40476259 · Full text
In this editorial, we comment on the article by Sá-Oliveira . We focus specifically on the role of platelet-rich fibrin (PRF) in modulating innate immunity to enhance wound repair. The process of wound healing is complex...
In this editorial, we comment on the article by Sá-Oliveira . We focus specifically on the role of platelet-rich fibrin (PRF) in modulating innate immunity to enhance wound repair. The process of wound healing is complex and involves a coordinated series of biological events, including inflammation, cell proliferation, and tissue remodeling. The innate immune system is important in the early stages of wound repair, with inflammation being a crucial initial phase in tissue regeneration. However, the inflammatory response should be regulated, as excessive or dysregulated inflammation can impair healing. Platelet concentrates, specifically PRF, have originated as promising tools to optimize the tissue repair process. PRF is a second-generation platelet concentrate, and the release of growth factors (GFs) plays a determining role in several aspects of wound healing, including promoting cell proliferation, stimulating angiogenesis, and modulating inflammation. PRF forms a fibrin matrix that entraps platelets and GFs. This structure allows for their sustained release over time, which is believed to provide a more favorable microenvironment for tissue repair. Recent research by Sá-Oliveira has provided valuable evidence supporting the efficacy of PRF in promoting wound healing. Their study, conducted on an animal model, demonstrated that PRF-based dressings were more effective in accelerating wound closure in the early stages of the healing process, enhancing tissue repair, and modulating the inflammatory response. We explore how PRF's unique properties contribute to a more controlled and effective healing process. By examining these findings, we aim to highlight PRF's potential as a promising therapeutic strategy for improved wound management.
Stem cell therapy for Parkinson's disease: A new hope for neural regeneration.
Mokhtari YG, Varnava I, Kyrgiannis K … +2 more , Ampatsidou V, Giakoumettis D
World J Biol Chem · 2025 Jun · PMID 40476258 · Full text
Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the loss of dopaminergic neurons in the substantia nigra that leads to reduced dopamine levels and impaired motor function. Current treatment...
Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the loss of dopaminergic neurons in the substantia nigra that leads to reduced dopamine levels and impaired motor function. Current treatments only provide temporary symptom relief without addressing the underlying neuronal loss. A promising new approach for treating PD is stem cell therapy, particularly induced pluripotent stem cells and human pluripotent stem cells. They have the ability to differentiate into various neural cells, offering potential for neuronal replacement and restoration of brain function. Induced pluripotent stem cells are derived from reprogramming adult cells and present advantages such as genetic compatibility and reduced immune rejection, overcoming ethical concerns associated with embryonic stem cells. Preclinical studies show promising results, demonstrating that stem cells can differentiate into dopaminergic neurons and improve motor function in animal models. These advancements pave the way for clinical trials and potential long-term solutions for patients with PD. This review highlighted the significance of stem cell therapy in neuroregeneration and addressed preclinical successes, challenges in long-term safety, and ethical considerations, with the hope of revolutionizing PD treatment and improving patient outcomes.
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